• folds of Kerkring/plicae circulares
• villi/crypts
• microvilli

• fasting- very little space
• absorptive- space opens up

• as sodium movement pulls water passively, water carries addition sodium and other ions by convection

• luminal osmolality
• rate of active solute transport (standing osmotic gradient model) (increases in fecal water always secondary to increases in fecal solute)
• bowel segment

• active transport of sodium out of the cell into intermembrane space (where tight junction is nearby) creates an osmotic gradient for water to come into these space

• villus
  • abundant in brush border hydrolases
  • high nutrient transport
  • site for water absorption
  • low permeability
• crypts
  • site for water secretion (not much nutrient transport)
  • high permeability

• duodenum and jejunum- absorb a high volume with a low efficiency (I could take in 9 L and only have 5.5 L absorbed)
• ileum and colon- absorb a low volume at a high efficiency (I could have 3.5 L left and absorb 3.3)

• passive permeability will decrease as we move down the intestines
  • duodenum/jejunum
    • largest radius
    • highest permeability with low resistance
  • ileum
    • moderate radius
    • moderate permeability with moderate resistance
  • colon
    • lowest radius
    • lowest permeability with highest resistance

• hypertonic meals (MOST COMMON)- we add water to this meal, making it isotonic
• hypotonic meals- we remove water from this meal, making it isotonic

This happens in the duodenum.

• transcellular passive (via negative potential within the cell)
  • energy given by 3Na/2K pump'
• substrate coupled transport
• electroneutral transport
  • Na/H antiport
  • Na/Cl cotransport

• inhibits electroneutral transport
  • Na/H antiport
  • Na/Cl cotransport
  • Cl/HCO3 antiport

Clinical app.- cholera increases cAMP, so it decreases neutral Na/Cl reabsorption

1. calcium diffuse into cell
2. stimulates synthesis of Vitamin D3 in PCT of kidney via PTH
3. stimulates synthesis of calcium binding protein (calbindin)
4. calbindin binds to calcium
5. calcium actively pumped out of cell into blood

• neutral transport happens mainly in fasting
• cholera activates cAMP which inhibits neutral transport by increasing cAMP
• cholera is mainly prevalant in developing nations, where starvation can occur
• if the people are not eating, and their main absorptive mechanism is being attacked, their diarrhea is much worse

1. heme-iron is uptaken ino cell
2. heme is separated from iron by lysosomal enzymes, leaving free iron
3. iron binds to apoferritin to form ferritin
4. iron dissociates from ferritin, binds to mobilferrin and is transported into blood
5. iron binds to transferrin, now it can be transported in the blood to storage and utilization sites

amount of transferrin (NOTE: uptake is not very efficient in the epithelial cells)

• deficiency
  • increase transferrin production
  • increase uptake from lumen
  • smaller loss when enterocytes sloughed off
• overload
  • decrease transferrin production
  • decrease uptake from lumen
  • larger loss in stool when iron sloughed off
    • cause dark color to stool

• increased thickening of crypts
• decrease in number of villi

Classic in celiac disease.

• oral rehydrating solutions
  • contain glucose and starch
  • the Na/substrate transport is not affected by cholera
  • allows for effective rehydration of the individual even though cholera is still active

• small intestines
  • glucose
  • AA's
• large intestines
  • short chain fatty acids
  • bile salts

• small intestines- NO EFFECT
• large intestines- increased sodium absorption, increased potassium secretion

• along with sodium in Na/Cl cotransport
• paracellular via lumen potential difference between lumen and blood

• in colon and terminal ileum
  1. H2O and CO2 form H2CO3 via CA
  2. dissociates into H and HCO3
  3. HCO3 goes into lumen via HCO3/Cl antiport
     1. neutralizes acid products from bacterial flora
     2. Cl then goes into blood

• sodium drives absorption
• chlorid drives secretion

• ileum
• colon
• rectum

• absorption- the entire gut (active absorption only in the distal colon and rectum)
• secretion- colon and rectum (this is where active secretion occurs as well)

1. alpha 1,4 links broken by salivary and pancreatic amylase by the time we get to the duodenum (intraluminal) to form:
   1. maltotriose
   2. alpha limit dextrin
   3. maltose
2. the disaccharides and oligosacharides are broken down by brush border enzymes
   1. maltase
   2. sucrase
   3. lactase
   4. dextrinase
3. forms:
   1. glucose
   2. galactose
   3. fructose
4. monosaccharides taken up into cell via SGLT1 transporter (sodium dependent) and GLUT5 (fructose)
   1. but if high sugar diet, GLUT will be found on the luminal surface of cell
   2. RATE LIMITING STEP
5. exit cell via GLUT2 transporter and go into the capillaries

normally, all by the mid-jejunum

(except: lactose with those who are lactose intolerant)

1. pepsin activated along with pancreatic proteases
2. converts proteins into oligopeptides and AA's
3. uptake into the cell via Na dependent mechanism (there is a H cotransport as well for oligopeptides)
   1. RATE LIMITING STEP
   2. small intestines prefers to take up oligopeptides
4. oligosaccharides converted to AA's via cytoplasmic peptidases
5. exit cell via facilitated diffusion

• most absorption in the jejunum, but some can happen in ileum, but happens throughout the whole course of the small intestines

1. B12 binds to salivary haptocorrin
2. pancreatic proteases will cleave off haptocorrin in the small intestines
3. IF binds to B12
4. B12 dissociates from IF and is absorbed into portal circulation at terminal ileum

Unique: most water soluble vitamins absorbed in the upper small intestines.

1. when fat droplet goes into duodenum, bile salts are released
2. bile salts will take the fat droplet and emulsify into digestible micelles
3. enzymes will act at the outer interface
   1. TAG's broken into MAG and free FA's via lipase and colipase
   2. lecthin/phospholipids broken into lysolecthin and free FA's via calcium, bile salts, phospholipase A2
   3. cholesterol esters are broken into free cholesterol and free FA's via cholesterol esterase
4. bile salts allow micelles formed to get into the unstirred water layer of the enterocyte
   1. RATE LIMITING STEP
5. free fatty acids and MAG's are delivered to the cell via diffusion
6. TAG's are re-made
7. add apoproteins to the TAG's to form chylomicrons
8. diffuse into central lacteals of lymphatic system

• lipase is not active without colipase
  • colipase is secreted as a proenzyme from the pancrease
  • it prevents the bile salts from inactivation lipase so lipase can continue to break down TAG's

• ileal break
  • PYY released
    • slow gastric acid secretion
    • slow gastric emptying
    • slow pancreatic secretion
    • slow transit rate
    • decrease colonic motility

• protein
• carbohydrates
  • (unless they are not absorbed in small intestines, in which case they would be converted to fatty acids via bacterial fermentation)

• absorbes the SCFA and the bacterial lipases hydrolyze the fatty acid esters

• bile acids go into colon if not absorbed in the ileum
• they enter the colon and are metabolized by the bacterial flora
  • inhibit sodium and water reabsorption in proximal colon

• swallowed air
• carbon dioxide
• volitale fatty acids (bacterial digestion bproduct)
• diffusion of gas from blood to lumen
• bacteria (MAIN SOURCE)
  • hydrogen (seen in breath of those who are lactose intolerant)
  • methane
  • carbon dioxide
• nitrogen

• moves slowly through gut (slower gastric emptying
  • clinical application- good treatment for constipation

• moves quickly through gut (increase gastric emptying)
  • clinical app.- good for colonic health

• fiber takes loner to eat and stays in the stomach longer
• fiber buffers acid in stomach, altering gastrin release
• viscous fibers can inerfere with absorption of nutrients at the small intestines